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control-odn1826  (Gene Design Inc)

 
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    Gene Design Inc control-odn1826
    TLR9 activation promoted TNF-α expression in macrophages. (A) Activation of TLR9 by <t>ODN1826</t> (0.1-1.0 μM) for 4 h promoted the expression of TNF-α in wild-type macrophages but not in Tlr9 −/− macrophages ( N = 4, per group). (B) Wild-type or Tlr9 −/− macrophages were treated with plasma obtained from wild-type mice which received femoral ligation or sham operation for 4 h. Plasma from mice with ischemic muscle increased TNF-α expression in wild-type macrophages compared with that from sham-operated mice, however, plasma from mice with ischemic muscle did not show this response in Tlr9 −/− macrophages ( N = 4-6, per group). (C) ODN1826 promoted degradation of IκBα in wild-type macrophages in time dependent manner, suggesting the activation of NF-κB signaling. In Tlr9 −/− macrophages, this response was not observed. * P < 0.05 and *** P < 0.001. All values are mean ± SEM.
    Control Odn1826, supplied by Gene Design Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/control-odn1826/product/Gene Design Inc
    Average 90 stars, based on 1 article reviews
    control-odn1826 - by Bioz Stars, 2026-03
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    Images

    1) Product Images from "Activation of Toll-Like Receptor 9 Impairs Blood Flow Recovery After Hind-Limb Ischemia"

    Article Title: Activation of Toll-Like Receptor 9 Impairs Blood Flow Recovery After Hind-Limb Ischemia

    Journal: Frontiers in Cardiovascular Medicine

    doi: 10.3389/fcvm.2018.00144

    TLR9 activation promoted TNF-α expression in macrophages. (A) Activation of TLR9 by ODN1826 (0.1-1.0 μM) for 4 h promoted the expression of TNF-α in wild-type macrophages but not in Tlr9 −/− macrophages ( N = 4, per group). (B) Wild-type or Tlr9 −/− macrophages were treated with plasma obtained from wild-type mice which received femoral ligation or sham operation for 4 h. Plasma from mice with ischemic muscle increased TNF-α expression in wild-type macrophages compared with that from sham-operated mice, however, plasma from mice with ischemic muscle did not show this response in Tlr9 −/− macrophages ( N = 4-6, per group). (C) ODN1826 promoted degradation of IκBα in wild-type macrophages in time dependent manner, suggesting the activation of NF-κB signaling. In Tlr9 −/− macrophages, this response was not observed. * P < 0.05 and *** P < 0.001. All values are mean ± SEM.
    Figure Legend Snippet: TLR9 activation promoted TNF-α expression in macrophages. (A) Activation of TLR9 by ODN1826 (0.1-1.0 μM) for 4 h promoted the expression of TNF-α in wild-type macrophages but not in Tlr9 −/− macrophages ( N = 4, per group). (B) Wild-type or Tlr9 −/− macrophages were treated with plasma obtained from wild-type mice which received femoral ligation or sham operation for 4 h. Plasma from mice with ischemic muscle increased TNF-α expression in wild-type macrophages compared with that from sham-operated mice, however, plasma from mice with ischemic muscle did not show this response in Tlr9 −/− macrophages ( N = 4-6, per group). (C) ODN1826 promoted degradation of IκBα in wild-type macrophages in time dependent manner, suggesting the activation of NF-κB signaling. In Tlr9 −/− macrophages, this response was not observed. * P < 0.05 and *** P < 0.001. All values are mean ± SEM.

    Techniques Used: Activation Assay, Expressing, Ligation

    TLR9-induced macrophage activation accelerated cell death of HUVEC. (A) HUVEC were treated with the CM obtained from wild-type or Tlr9 −/− macrophages treated with ODN1826 or control-ODN1826. At 72 h after treatment, the viability of HUVEC determined by MTS assay was significantly reduced by CM obtained from wild-type macrophage activated by ODN1826, although the viability of HUVEC was not affected by CM obtained from Tlr9 −/− macrophage ( N = 5, per group). (B) Stimulation with TNF-α for 24 h decreased cell viability in HUVEC as determined by MTS assay ( N = 4-6, per group). * P < 0.05 and ** P < 0.01. All values are mean ± SEM.
    Figure Legend Snippet: TLR9-induced macrophage activation accelerated cell death of HUVEC. (A) HUVEC were treated with the CM obtained from wild-type or Tlr9 −/− macrophages treated with ODN1826 or control-ODN1826. At 72 h after treatment, the viability of HUVEC determined by MTS assay was significantly reduced by CM obtained from wild-type macrophage activated by ODN1826, although the viability of HUVEC was not affected by CM obtained from Tlr9 −/− macrophage ( N = 5, per group). (B) Stimulation with TNF-α for 24 h decreased cell viability in HUVEC as determined by MTS assay ( N = 4-6, per group). * P < 0.05 and ** P < 0.01. All values are mean ± SEM.

    Techniques Used: Activation Assay, MTS Assay



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    Image Search Results


    TLR9 activation promoted TNF-α expression in macrophages. (A) Activation of TLR9 by ODN1826 (0.1-1.0 μM) for 4 h promoted the expression of TNF-α in wild-type macrophages but not in Tlr9 −/− macrophages ( N = 4, per group). (B) Wild-type or Tlr9 −/− macrophages were treated with plasma obtained from wild-type mice which received femoral ligation or sham operation for 4 h. Plasma from mice with ischemic muscle increased TNF-α expression in wild-type macrophages compared with that from sham-operated mice, however, plasma from mice with ischemic muscle did not show this response in Tlr9 −/− macrophages ( N = 4-6, per group). (C) ODN1826 promoted degradation of IκBα in wild-type macrophages in time dependent manner, suggesting the activation of NF-κB signaling. In Tlr9 −/− macrophages, this response was not observed. * P < 0.05 and *** P < 0.001. All values are mean ± SEM.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Activation of Toll-Like Receptor 9 Impairs Blood Flow Recovery After Hind-Limb Ischemia

    doi: 10.3389/fcvm.2018.00144

    Figure Lengend Snippet: TLR9 activation promoted TNF-α expression in macrophages. (A) Activation of TLR9 by ODN1826 (0.1-1.0 μM) for 4 h promoted the expression of TNF-α in wild-type macrophages but not in Tlr9 −/− macrophages ( N = 4, per group). (B) Wild-type or Tlr9 −/− macrophages were treated with plasma obtained from wild-type mice which received femoral ligation or sham operation for 4 h. Plasma from mice with ischemic muscle increased TNF-α expression in wild-type macrophages compared with that from sham-operated mice, however, plasma from mice with ischemic muscle did not show this response in Tlr9 −/− macrophages ( N = 4-6, per group). (C) ODN1826 promoted degradation of IκBα in wild-type macrophages in time dependent manner, suggesting the activation of NF-κB signaling. In Tlr9 −/− macrophages, this response was not observed. * P < 0.05 and *** P < 0.001. All values are mean ± SEM.

    Article Snippet: Peritoneal macrophages were stimulated with ODN1826 or control-ODN1826 (GeneDesign, Inc.), synthetic oligonucleotides that contain unmethylated CpG, for indicated time.

    Techniques: Activation Assay, Expressing, Ligation

    TLR9-induced macrophage activation accelerated cell death of HUVEC. (A) HUVEC were treated with the CM obtained from wild-type or Tlr9 −/− macrophages treated with ODN1826 or control-ODN1826. At 72 h after treatment, the viability of HUVEC determined by MTS assay was significantly reduced by CM obtained from wild-type macrophage activated by ODN1826, although the viability of HUVEC was not affected by CM obtained from Tlr9 −/− macrophage ( N = 5, per group). (B) Stimulation with TNF-α for 24 h decreased cell viability in HUVEC as determined by MTS assay ( N = 4-6, per group). * P < 0.05 and ** P < 0.01. All values are mean ± SEM.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Activation of Toll-Like Receptor 9 Impairs Blood Flow Recovery After Hind-Limb Ischemia

    doi: 10.3389/fcvm.2018.00144

    Figure Lengend Snippet: TLR9-induced macrophage activation accelerated cell death of HUVEC. (A) HUVEC were treated with the CM obtained from wild-type or Tlr9 −/− macrophages treated with ODN1826 or control-ODN1826. At 72 h after treatment, the viability of HUVEC determined by MTS assay was significantly reduced by CM obtained from wild-type macrophage activated by ODN1826, although the viability of HUVEC was not affected by CM obtained from Tlr9 −/− macrophage ( N = 5, per group). (B) Stimulation with TNF-α for 24 h decreased cell viability in HUVEC as determined by MTS assay ( N = 4-6, per group). * P < 0.05 and ** P < 0.01. All values are mean ± SEM.

    Article Snippet: Peritoneal macrophages were stimulated with ODN1826 or control-ODN1826 (GeneDesign, Inc.), synthetic oligonucleotides that contain unmethylated CpG, for indicated time.

    Techniques: Activation Assay, MTS Assay